Journal
NATURE IMMUNOLOGY
Volume 14, Issue 9, Pages 949-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2682
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Funding
- US National Institutes of Health [AI072690, AI088427, HL018208, HL087088, AI089079]
- American Heart Association [11SDG7520018]
- National Institute of Allergy and Infectious Diseases
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Leukocytes must traverse inflamed tissues to effectively control local infection. Although motility in dense tissues seems to be integrin independent and based on actomyosin-mediated protrusion and contraction, during inflammation, changes to the extracellular matrix (ECM) may necessitate distinct motility requirements. Indeed, we found that the interstitial motility of T cells was critically dependent on Arg-Gly-Asp (RGD)-binding integrins in the inflamed dermis. Inflammation-induced deposition of fibronectin was functionally linked to higher expression of integrin alpha(V) on effector CD4(+) T cells. By intravital multiphoton imaging, we found that the motility of CD4(+) T cells was dependent on alpha(V) expression. Selective blockade or knockdown of alpha(V) arrested T helper type 1 (T(H)1) cells in the inflamed tissue and attenuated local effector function. Our data demonstrate context-dependent specificity of lymphocyte movement in inflamed tissues that is essential for protective immunity.
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